1. Field of the Invention
The present invention pertains to heart tachycardia, and more particularly, relates to ventricular tachycardia termination.
2. Description of the Prior Art
The basic concept of anti-tachycardia pacing was invented by Zacouto in the late 1960s. There have been many patents on traditional anti-tachycardia pacing. Examples are: U.S. Pat. No. 4,312,356 to Sowton; U.S. Pat. No. 4,390,021 to Spurrell; U.S. Pat. No. 4,398,536 to Nappholz; U.S. Pat. No. 4,408,606 to Spurrell; U.S. Pat. No. 4,488,554 to Nappholz; and U.S. Pat. No. 4,577,633 to Berkovitz.
No one has come close to the present concept of delivering multiple-pulse anti-tachycardia therapy through the defibrillation electrodes. Shenasa from Switzerland contributed an abstract at the American Heart Association meeting in 1991, Circ. Vol. 84, No. 4, p. II-426 (October, 1991 in which he applied very low voltages, under one volt, to defibrillation electrodes. He characterized these voltage as "sub-threshold stimulation" levels, and applied them at extremely high rates (50-millisecond pulses at the rate of 1200/minute). Shenasa's philosophy was to numb the myocardial cells near the electrodes in order to make these cells less likely to sustain the re-entrant loop of the ventricular tachycardia. He reported only a 52% success rate in treating tachycardia arrhythmias using this methodology. A
U.S. Pat. No. 4,996,984, issued to Sweeney discloses the use of a pair (or more) of pulses for defibrillation. However, they were addressing fibrillation and not tachycardia. Also they were using pulses with just slightly less energy than conventional defibrillation pulses--on the order of 10 joules. Their work was inspired by the 20-year-old work of the Swedish researcher Kugelberg, who used trains of high-energy pulses to defibrillate.
In addition to the standard anti-tachycardia pacing of the prior art using the pacing electrodes on a standard cardiac catheter, there is another accepted technique for abolishing ventricular tachycardias. It is known as cardioversion, and involves the delivery of a single pulse through large-area defibrillation electrodes. Such a pulse usually has an energy in the neighborhood of one joule. This value is well above that of a pacing pulse, but far below that of a typical defibrillation pulse. While the present invention also uses defibrillation electrodes for terminating tachycardia, it is distinct from the prior art in using two or more pulses, and more wide-ranging energy values.
Ventricular tachycardia is a racing of the ventricle. The most accepted theory is that there exists a closed loop of myocardium with a diameter on the order of 1 cm, as illustrated in FIG. 1. That is, the path of cell stimulation is circular, with a path length (circumference) sufficient to permit a given cell to "repolarize", or to recover from the previous stimulation, before the wave of stimulation comes around the circle the next time. In biomedical terminology, such a closed loop is described as a "reentrant" loop, terminology that will be used below. The adjective generically identifies a situation wherein a path of adjacent-cell stimulation closes on itself, or "reenters" a previous path. In the loop case, the activated cells continue to activate cells in a counterclockwise rotation in continuous fashion. Immediately behind the cells just stimulated are cells that are fairly "refractory" or resistant to stimulation having not fully recovered from activation. Farther behind them are cells that are fully recovered (repolarized), and hence, are amenable to stimulation or reactivation.
This kind of "single-source" ventricular tachycardia generates a rather consistently shaped electrical signal, and hence, is referred to as a "monomorphic ventricular tachycardia". If there are more sources involved, then the arrhythmia is referred to as a "polymorphic ventricular tachycardia".
The presently accepted method of anti-tachycardia pacing is to pace at a remote location of the heart at a rate slightly higher than the ventricular tachycardia rate. The pacing pulse is delivered through conventional pacing electrodes that are essentially small point sources, a choice made to minimize the energy required to stimulate the closest neighboring cells. The activation pulse wave then spreads through the myocardium towards the re-entrant loop. It is desired that one of the pulses will arrive in the correct phase and will stimulate the cells of the loop that have recovered fully from activation. If this happens, then these cells will be refractory to the loop activation, and hence, the ventricular tachycardia will terminate.
This is weakly analogous to lighting a back-fire to stop a forest fire. The weakness in the analogy is that a forest fire does not repeatedly sweep the same area, and thus, does not give multiple opportunities for extinction or reignition.
There are several timing problems that prevent a 100% success rate with this technique. The major problem is that the pulse wave must arrive at the nearest side of the reentrant loop while it is in repolarization, or amenable to activation. Before it can do this, the wave must progress through myocardium without being annihilated by the activation waves emanating from the loop itself. (Recall that the loop is generating expanding activation waves throughout the myocardium in a fashion similar to the waves from a pebble dropped into the center of a smooth pond.) This problem is illustrated in FIG. 2. There is seen the wave at the lower left emanating from the pacing electrodes often one of the anti-tachycardia pulses was delivered. In an intermediate region, it competes with the wave launched by the reentrant loop responsible for the tachycardia, and has a fair probability of being annihilated.
The anti-tachycardia pacing of the prior art has been reported to work 50% to 90% of the time in cases of monomorphic ventricular tachycardia, with the chief problem being the critical timing constraints. This limited success in the prior art is bad enough, but the situation is actually worse. The series of pulses employed sometimes causes a higher-rate monomorphic ventricular tachycardia, or pulse-rate "acceleration". This can result in patient unconsciousness, or can require a painful high-energy shock for termination. Added to these problems for the monomorphic case, we must add that for cases of multiple loops (or sources), the prior art therapy has essentially no chance of working.
The prior art technique of anti-tachycardia pacing uses a burst of, for example, ten pulses at a rate slightly higher than the ventricular-tachycardia rate in hopes of abolishing it. Sometimes, pulse-rate "scanning" is employed in an effort to hit the correct rate. In scanning, the pacing valve is increased with every burst. In another prior art technique, "ramping" the rate is increased during the burst. The prior art chooses a higher rate of pacing because the pacing pulses will vary in phase with respect to the ventricular tachycardia, and thus, there is an increased opportunity for the pacing wave to arrive at a repolarized portion of the re-entrant loop before the pacing wave is itself annihilated.
The situation can be summarized in somewhat different words as follows. The high pulse rate in monomorphic tachycardia is a consequence of a signal circulating in a small-diameter closed loop at some location on the myocardium. The prior art therapy delivers a short series of pacing pulses at a rate higher than that of the tachycardia. The point of using the higher rate in therapy is so that as the wave launched by each therapeutic pulse arrives at the nearest edge of the loop, the chance of having such a wave's arrival coincide with having the repolarized (or stimulation-amenable) zone present at the nearest edge is increased; that is, one of the pulse waves from the short train will have a fair probability of arriving at just the right instant. (The geometrical situation can be appreciated from FIGS. 1 and 2.) Further, the point of using a burst of pulses, rather than a long series, is to provide a quiet interval after therapy during which dominance can be reestablished by waves coming from the pacemaker (whether from the heart's natural pacing center, or from the electrodes of a prosthetic pacemaker). The foregoing description explains the often indifferent results obtained using prior art anti-tachycardia methods, even in the simplest monomorphic case. The pulse waves may not arrive at the right time, may be annihilated by tachycardia waves, as in FIG. 2, and may induce even more serious conditions.